Introduction
The plague of type 2 diabetes has swept the nation and in the United States about 7.8% of the population is diabetic (Zhang, Lee, Cowan, Fabsitz, & Howard, 2011). Today, more than ever, new diets and quick fixes are heavily marketed to help shed some light on losing weight and preventing type 2 diabetes. Interestingly, one of the most widely consumed beverages in the United States has recently been shown to enhance insulin sensitivity and prevent diabetes.
The purpose of the review is to determine the impact of coffee consumption and the progression of type 2 diabetes. Major topics being reviewed are: insulin resistance and glucose metabolism. In section I, a brief overview of type 2 diabetes is presented and additional information of caffeine’s impact on human metabolism. In section II, research of coffee and type 2 diabetes prevalence has been complied and compared. Section III, summarizes the relationship between coffee and type 2 diabetes and mechanisms associated.
Section I: Brief Overview of Caffeine & Metabolism
Type 2 diabetes mellitus is characterized by the combination of insulin resistance and the decreased functioning of pancreatic B-cells that secrete insulin in response to glucose. (Li & Hui, 2009) Insulin sensitivity is reflected by the amount of glucose uptake by a given insulin concentration (McArdle, Katch, & Katch, 2006). Type 2 diabetes increases the risk of other chronic diseases, such as hypertension, dyslipidemia, and cardiovascular disease (Pimentel, Zemdegs, Theodoro, & Mota, 2009).
More than half of Americans consume coffee and it is one of the most widely consumed beverages in the world (Sartorelli et al., 2010). The average American coffee consumption is about 2 cups per day and it has been associated with lowering the risk of type 2 diabetes. (Zhang et al., 2011) Coffee is brewed of different components that may alter glucose metabolism, including caffeine, phenolic cholorogenic acid, magnesium, and other minerals, antioxidants, and vitamins (Pimentel et al., 2009). One of the primary substances in coffee would be caffeine and it increases basal metabolic rate and thermogenesis (Oba et al., 2010). In western societies, the average daily caffeine intake is about 300 mg and the recommended adult intake is about 400 mg/day (Pimentel et al., 2009). Another primary substance in a cup of coffee would be chlorogenic acid and it has shown antioxidant properties (Sartorelli et al., 2010). In an 8 fl oz cup of this popular beverage, there is about 7 mg of magnesium, which has been related to glucose metabolism and improved insulin sensitivity (Loopstra-Masters, Liese, Haffner, Wagenknecht, & Hanley, 2010; Pimentel et al., 2009). Some studies have shown that coffee has an effect to decrease the prevalence of type 2 diabetes and other studies have shown the adverse affect. In this review, the following association was investigated to determine the relationship between coffee intake and mechanisms that may reduce the occurrence of type 2 diabetes.
Section II: Research
In a study from Takayama, Japan, the prevalence of diabetes to the consumption of coffee and other beverages and food containing caffeine was compared, among 5897 men and 7643 women. In 1992, the consumption of coffee, green tea, oolong tea, black tea, and chocolate snacks were measured using a semi-quantitative FFQ. Then in 2002, a follow-up survey was used to report the prevalence of diabetes; 278 men and 175 women reported to develop diabetes during this time. According to the findings, younger age, high levels of education (12 years or more), and cigarette smoking was associated with higher coffee consumption. Total energy intake and carbohydrate intake were higher with an increased level of coffee and soda consumption. Correlation coefficient analysis between caffeine intake and body mass index (BMI) showed no clear correlation both among men and women. There was a modest inverse relationship, but not significant, and the results implied that coffee consumption decreased the risk of diabetes (Oba et al., 2010).
In another study, the purpose was to determine the cross-sectional relationship between coffee consumption, either caffeinated or decaffeinated, and measures of insulin sensitivity and secretion by acute insulin response (AIR) in the United States. It consisted of nondiabetic adults (n= 954) from the Insulin Resistance Atherosclerosis Study (IRAS). The following measurements were used: intravenous glucose tolerance test (FSIGT), 2-hr postload glucose measured by OGTT, fasting insulin, and proinsulin to C-peptide ratios. It was found that caffeinated and decaffineated intakes inversely correlated (r= -0.20, p <0.0001). The highest coffee consumption was observed in African Americans, smokers, and participants with the highest mean energy intake.
According to the findings, the lowest proportion of participants with IGT was observed in the highest coffee intake category. Caffeinated coffee intake was not associated with acute insulin response or proinsulin ratios. Caffeinated coffee was associated with a significant 13% decreased odds of having IGT with the minimally adjusted model (p= 0.04); 16% decreased odds in the fully adjusted models (p= 0.0003). It was found that caffeinated coffee was positively related to insulin sensitivity (B= 0.054, p= 0.04) and inversely related to 2-hour postload glucose (r= -0.37, p= 0.0003) in all the regression models. In comparison, decaffeinated coffee intake was inversely related to 2-hour postload glucose (r= -0.47, p= 0.0096) and both intact (r= -0.15) and split (r= -0.25) proinsulin to C-peptide ratios; it was positively related to acute insulin response (r= 0.19, p= 0.0132). This related decaffeinated coffee intake to measures of beta cell function. Limitations for the study were that it was a cross-sectional, relied on FFQ estimations of serving size, and the time of day the coffee was consumed was not collected. In the study, there was a narrow range of coffee consumption, about 78% of the participants consumed less than one cup of coffee daily (Loopstra-Masters et al., 2010).
In another study that was conducted for 8 weeks, between May 2006 and September 2008, it was a randomized design and all participants were overweight volunteers (n= 65), the mean age of the participants was 40, and the mean BMI was 29.5 kg/m2. Out of the participants, 11 did not qualify and 9 withdrew; participants were excluded if there were on medications, breastfeeding, or planning on pregnancy. Prior to the study, the participants consulted a Registered Dietician and after 2 weeks of caffeine washout and overnight fast, participants attended baseline assessments. Participants were assigned to: the control group (no coffee) or one of the two coffee groups (decaffeinated or caffeinated). They were instructed to maintain stable exercise and diets, and keep 3-day food diaries. The measurements were taken at: baseline, 4 week and 8 week visit.
According to the findings, when compared to the control group, the consumption of caffeinated coffee group had significantly higher adiponectin (increased by 1.44 ug/mL from baseline; CI: 0.23, 2.66) and IL-6 (60% difference; CI: 8, 138); the decrease in fetuin A was not statistically significant. When evaluating blood pressure and blood lipids, participants in the decaffeinated group had a lower systolic by 3.1 mmHg and significantly lower diastolic by 5.7 mmHg (CI: -10.9, -0.6), in comparison with those in the control group. There was no significant difference between the three treatment groups for C-reactive protein (CRP) or measures of glucose metabolism. Overall, it can be suggested that changes in adiponectin and slight changes in fetuin A levels may be associated with improvements in adipocyte and liver function. This may contribute to beneficial metabolic effects of long-term coffee consumption (Wedick et al., 2011).
To determine the association between coffee consumption and type 2 diabetes on American Indians, the longitudinal study used American Indians from the Strong Heart Study. The sample population consisted of participants between the ages of 45 and 74 years from 13 tribes (n= 4549 total; n= 1141 at risk). Baseline examinations from 1989-1992 were conducted with personal interviews with each participant; the amount of caffeinated beverages estimated. During the second follow-up, a 24-hour dietary recall was used to determine the proportion of different participants consumed. It was found that consumption of tea, cocoa, or chocolate milk were very low, and 97.5% of the primary consumption was coffee. According to the findings, the consumption of 12 or more cups of coffee per day was associated with a significant reduction in the incidence of diabetes, when compared with those who did not drink coffee, approximately 67% and the hazard ratio for diabetes of 0.33 (p= 0.02). The levels of coffee consumption were directly related to current smoking; it was inversely related to BMI, waist circumference, female, and hypertension. Limitations to this study would be the lack of dietary data and other unmeasured cofactors (Zhang et al., 2011).
In a cohort study, French women between the ages of 41 and 72 years, diabetic and non-diabetic (n=98,995) were used to investigate the association between coffee and risk of diabetes. During 1993 and 1995, a diet-history questionnaire was used to assess food and drink intakes and in 2007 the last available questionnaire was completed. In order to compare the timing of coffee consumption, six separate models were used at six different times of the day. The different types of coffee were: regular and decaffeinated coffee, filtered and instant coffee, black coffee and coffee with milk, and coffee with and without sugar. It was found that 71% of the women drink coffee at lunchtime and lunch was the highest source of daily nutrients, followed by dinner and breakfast. Overall, younger, cigarette smoking, and higher mean BMI measurements were all associated with the highest coffee consumers. There was no significant correlation between coffee or caffeine intake and the risk of diabetes. Comparing no coffee to high coffee intake (3 cups/day) showed a lower diabetes risk and the hazard ratio was 0.73 (CI: 0.61, 0.87; p= <0.0001). An inverse relationship between coffee consumption and the risk of diabetes was suggested (Sartorelli, et al., 2010).
In another study, the effect of increasing coffee on: serum markers of subclinical inflammation, oxidative stress, lipids, and glucose metabolism; the effect on insulin resistance, immune mediator levels, and the use of methylxanthine and polyphenol concentrations as coffee intake markers was investigated. The participants were all under the age of 65, non-diabetic, but at risk of developing type 2 diabetes. The study excluded participants on medications, specific diseases, drug or alcohol abuse, and breastfeeding or pregnant. The single-blind study had three stages and lasted 3 months. After each stage, glucose samples were measured following an overnight 8-hour fast. Stage one, participants did not drink coffee, stage two participants consumed 4 cups/day of coffee, and the last stage or third month 8 cups/day were consumed.
It was found that coffee biomarkers levels in the plasma were directly related to coffee consumption and there were no effects on glucose metabolism. When no coffee and 8 cups/day were compared, significant increases in total cholesterol by 12% (p=0.01), HDL by 7% (p=0.001), and apolipoprotein A-I by 4% (p=0.05) were found and there were significant decreases in the ratio of LDL to HDL by 8% and the ratio of apolipoprotein B to apolipoprotein A-I by 9%. Also, there was a modest increase in adiponectin concentrations (r= 0.442, p= 0.002), with increased coffee consumption of caffeine. Since, type 2 diabetes is associated with subclinical inflammation, the study suggests that long-term coffee consumption could reduce the risk of type 2 diabetes (Kempf et al., 2010).
Section III: Conclusion
It can be induced that there is an association between coffee consumption and type 2 diabetes. Even though some studies did not find the relationship significant, there were modest inverse relationships suggested. Limitations that may have interfered would be: the length of study, sample size, environmental, and dietary factors. Mechanisms that seem to benefit coffee drinkers would be the increase in adiponectin and the slight reduction in Fetuin A, which is a biomarker for inflammation and liver function. It has shown to impact on HDL cholesterol as well. Other interesting components that were found were that coffee consumption is related to younger age, high levels of education, and smoking. To further understand the relationship between coffee and type-2 diabetes, age would be an important component to control, since age is related to disease risk. In future studies, the timing of coffee consumption and impact on cholesterol should be further investigated. The timing of consumption is an important characteristic that may affect glucose metabolism and has not been investigated, except by Sartorelli et al. (2010). In the future, coffee consumption recommendations should be established for pre diabetic and diabetic states.
References
Kempf, K., Herder, C., Erlund, I., Kolb, H., Martin, S., Carstensen, M., et al. (2010).
Effects of coffee consumption on subclinical inflammation and other risk factors
for type 2 diabetes: a clinical trial. The American Journal of Clinical Nutrition ,
91, 950-957.
Loopstra-Masters, R., Liese, A., Haffner, S., Wagenknecht, L., & Hanley, A. (2010).
Associations between the intake of caffeinated and decaffeinated coffee and
measures of insulin sensitivty and beta cell function. Diabetologia , 54, 320-328.
Oba, S., Nagata, C., Nakamura, K., Kaori, F., Kawachi, T., & Shimizu, H. (2010).
Consumption of coffee, green tea, oolong tea, black tea, chocolate snacks, and the
caffeine content in relation to the risk of diabetes in Japanese men and women.
The British Journal of Nutrition , 103, 453-459.
Pimentel, G., Zemdegs, J., Theodoro, J., & Mota, J. (2009). Does long-term coffee intake
reduce type 2 diabetes mellitus risk. Diabetology & Metabolic Syndrome , 1 (6),
1-8.
Sartorelli, D., Fagherazzi, G., Balkau, B., Touillaud, M., Boutron-Ruault, M., Lauzon-
Guillain, B., et al. (2010). Differential effects of coffee on the risk of type 2
diabetes according to meal consumption in a French cohort of women: the
E3N/EPIC cohort study. The American Journal of Clinical Nutrition , 91, 1002-
1012.
Wedick, N., Brennan, A., Sun, Q., Hu, F., Mantzoros, C., & van Dam, R. (2011). Effects
of caffeinated and decaffeinated coffee on biological risk factors for type 2 diabetes: a randomized controlled trial. Nutrition Journal , 10 (93), 1-9.
Zhang, Y., Lee, E., Cowan, L., Fabsitz, R., & Howard, B. (2011). Coffee consumption
and the incidence of type 2 diabetes in men and women with normal glucose
tolerance: The Strong Heart Study. Nutrition, Metabolism & Cardiovascular
Diseases , 21, 418-423.
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